ArticlePLoS pathogens2015
Porphyromonas gingivalis evasion of autophagy and intracellular killing by human myeloid dendritic cells involves DC-SIGN-TLR2 crosstalk.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
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Who cites it
87 citing papers in PubMed, 111 citations in OpenAlex.
- The influence of vitamin D supplementation on local and systemic inflammatory markers in periodontitis patients: A pilot study.Oral diseases · 2019Trial
- Systemic Antibiotic Therapy Reduces Circulating Inflammatory Dendritic Cells and Treg-Th17 Plasticity in Periodontitis.Journal of immunology (Baltimore, Md. : 1950) · 2019Trial
- Cryo-EM structure of the native assembled Mfa type V pilus from the periodontal pathogen Porphyromonas gingivalis.Communications biology · 2026Article
- B cell immune response to Talaromyces marneffei infection in HIV-negative patients and rat models.BMC infectious diseases · 2026Article
- Microbial crosstalk along the oral-gut axis: organ-specific oncogenic adaptations of Porphyromonas gingivalis and Fusobacterium nucleatum.Neoplasia (New York, N.Y.) · 2026Review
- Periodontitis and Chronic Liver Disease: Mechanistic Insights Focusing onMicroorganisms · 2026Review
- Oral microbiota-driven immune modulation along the oral-gut axis: from local signals to systemic inflammation.NPJ biofilms and microbiomes · 2026Review
- Article
- Porphyromonas gingivalis promotes the formation and development of type 2 diabetes mellitus complicated with cognitive impairment by regulating gut microbiota and metabolic pathways.Molecular medicine (Cambridge, Mass.) · 2025Article
- Periodontopathogen-Related Cell Autophagy-A Double-Edged Sword.Inflammation · 2025Review
- Development of monoclonal antibodies againstmSphere · 2025Article
- Alzheimer's Disease andLife (Basel, Switzerland) · 2025Review
- Cell-Type-Specific ROS-AKT/mTOR-Autophagy Interplay-Should It Be Addressed in Periimplantitis?Diagnostics (Basel, Switzerland) · 2024Review
- Oral Pathobiont-Derived Outer Membrane Vesicles in the Oral-Gut Axis.International journal of molecular sciences · 2024Review
- Opportunistic pathogeniScience · 2024Article
- The role of autophagy in odontogenesis, dental implant surgery, periapical and periodontal diseases.Journal of cellular and molecular medicine · 2024Review
- Linking Periodontitis with Inflammatory Bowel Disease through the Oral-Gut Axis: The Potential Role ofBiomedicines · 2024Review
- Myeloid dendritic cells and periodontal disease association: integrated study of single-cell sequencing and Mendelian randomization analysis.Frontiers in immunology · 2024Article
- New Trends in the Impact of Periodontal Treatment on Early Cardiovascular Diseases Outcomes: Insights and Future Perspectives.Reviews in cardiovascular medicine · 2023Review
- Influence of Vitamin D on Periodontal Inflammation: A Review.Pathogens (Basel, Switzerland) · 2023Review
27 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
Signaling via pattern recognition receptors (PRRs) expressed on professional antigen presenting cells, such as dendritic cells (DCs), is crucial to the fate of engulfed microbes. Among the many PRRs expressed by DCs are Toll-like receptors (TLRs) and C-type lectins such as DC-SIGN. DC-SIGN is targeted by several major human pathogens for immune-evasion, although its role in intracellular routing of pathogens to autophagosomes is poorly understood. Here we examined the role of DC-SIGN and TLRs in evasion of autophagy and survival of Porphyromonas gingivalis in human monocyte-derived DCs (MoDCs). We employed a panel of P. gingivalis isogenic fimbriae deficient strains with defined defects in Mfa-1 fimbriae, a DC-SIGN ligand, and FimA fimbriae, a TLR2 agonist. Our results show that DC-SIGN dependent uptake of Mfa1+P. gingivalis strains by MoDCs resulted in lower intracellular killing and higher intracellular content of P. gingivalis. Moreover, Mfa1+P. gingivalis was mostly contained within single membrane vesicles, where it survived intracellularly. Survival was decreased by activation of TLR2 and/or autophagy. Mfa1+P. gingivalis strain did not induce significant levels of Rab5, LC3-II, and LAMP1. In contrast, P. gingivalis uptake through a DC-SIGN independent manner was associated with early endosomal routing through Rab5, increased LC3-II and LAMP-1, as well as the formation of double membrane intracellular phagophores, a characteristic feature of autophagy. These results suggest that selective engagement of DC-SIGN by Mfa-1+P. gingivalis promotes evasion of antibacterial autophagy and lysosome fusion, resulting in intracellular persistence in myeloid DCs; however TLR2 activation can overcome autophagy evasion and pathogen persistence in DCs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.